Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunodeficiency syndromes associated with protein-energy malnutrition (PEM) have been documented extensively, although to date the mechanism underlying these defects remains uncharacterized. In this study, we have evaluated T, B, and antigen-presenting cell functions of malnourished mice fed a 4% protein diet compared with litter-mate controls fed a 20% protein diet. Spleen cells from malnourished mice presented both soluble foreign protein and allogeneic MHC antigens less efficiently than control mice. However, T cells from malnourished animals demonstrated effective or enhanced specific T-cell activation when stimulated with allogeneic cells, while B cells from protein-deprived animals responded normally in proliferative responses to T-cell driven cognate and non-cognate, as well as mitogen, stimulation. To assess further antigen-presenting cell function, three requirements for successful antigen presentation were evaluated. First, the proliferation of the IL-1-dependent cloned T-cell line D10 demonstrated a slight deficiency in IL-1 production by malnourished splenic antigen-presenting cells, and the addition of saturating amounts of IL-1 to the assay could partially reconstitute function. Second, quantitative cell-sorter analysis revealed minimal deficiencies of spleen-cell Ia expression. Third, antigen-processing function was assayed in vitro by using processed antigen fragments; no improvement in protein-deprived antigen-presenting function resulted. Together, these findings suggest that either decreased Ia glycoprotein expression on a critical subset of antigen-presenting cells (APCs) or a quantitative deficiency in such a subset of cells, or both, underlie the defective antigen-presenting cell function observed in chronic protein deprivation (CPD).
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PMID:Defective antigen presentation in chronically protein-deprived mice. 313 Mar 10

The cell surface antigen associated with the transformed state of cells that could grow in an anchorage-independent manner was analyzed by use of techniques of DNA transfection and hybridomas secreting the monoclonal antibody (MoAb). Spleen cells of C57BL/6 mice immunized with a highly tumorigenic, chemically induced murine cultured colon 36 tumor (C-C36) of BALB/c origin were hybridized with NS-1, a hypoxanthine phosphoribosyltransferase-deficient myeloma line of BALB/c mice. Screening of hybridomas revealed an antibody that reacted with C-C36 and transformed Swiss 3T3 cells growing in soft agar after transfection of 3T3 cells with C-C36 DNA. The hybridomas that did not react with nontransformed 3T3 and the less tumorigenic BALB/c hemangioendothelioma line D10 were then selected. An MoAb was designated "#71295." This MoAb immunoprecipitated the antigen that consisted of 65,000- and 14,000-molecular-weight components with soluble C-C36 membrane antigens. It also reacted with 2 other chemically induced syngeneic colon tumor lines, cultured colon 26 tumor line and cultured colon 51 tumor line, and with fibrosarcoma Meth A. However, #71295 was not found in NS-1, D14, and BALB/c normal thymus, liver, colon, and kidney tissues. In addition, this MoAb could not inhibit the anchorage-independent growth of C-C36 and transformed 3T3 cells. These results suggest that although the molecule defined by #71295 might not be associated with the anchorage independence of cell growth, it could be a newly expressed determinant on the cell surface that is related to the events of cell transformation.
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PMID:Identification of transformation-related antigen by monoclonal antibody on Swiss 3T3 cells induced by transfection with murine cultured colon 36 tumor DNA. 346 94

An interleukin 1 alpha (IL-1 alpha) cDNA probe and an IL-1 responsive T-cell clone (D10.G4; half-maximal stimulation, 0.1-1 pM) have been used to study the production of IL-1 by primary murine cell populations, particularly macrophages and dendritic cells. Spleen and peritoneal macrophages produced IL-1 mRNA and released biologically active IL-1 when challenged with lipopolysaccharide (LPS). Induction of IL-1 was evident over a dose range of 0.01-10 micrograms of LPS per ml, and maximal mRNA levels were maintained from 4 to 20 hr. Several other stimuli did not induce IL-1 in cultured macrophages, including phorbol 12-myristate 13-acetate, gamma-interferon, Con A, macrophage colony-stimulating factor, IL-3, cachectin, and activated T cells. Activated T cells could markedly reduce the response of peritoneal macrophages to LPS. When other cell types were compared with macrophages, keratinocytes had high levels of IL-1 mRNA, apparently in response to endogenous LPS. However B and T lymphocytes did not yield detectable IL-1 during proliferative responses to LPS and Con A, respectively, while dendritic cells produced little or no IL-1 when challenged with a battery of stimuli. Therefore, IL-1 may not be required for the potent accessory function of dendritic cells in lymphocyte mitogenesis. The results indicate that macrophages and dendritic cells have different secretory capacities. The macrophage is the principal leukocyte that synthesizes IL-1, and select stimuli increase and decrease the levels of macrophage IL-1 mRNA.
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PMID:Induction of murine interleukin 1: stimuli and responsive primary cells. 349 97

Spleen cells from BALB/c mice immunized with MOPC 315 IgA were fused with P3X63/Ag8 myeloma cells. Hybrid clones were screened for antibody production by a plate-binding radioimmunoassay in which MOPC 315 IgA was reacted with culture supernatants and 125I-protein A. One antibody-producing hybridoma clone (D10) was selected and injected i.p. into BALB/c mice. Ascitic fluid of tum or-bearing animals reacted specifically with MOPC 315 IgA and the reaction was inhibited by DNP- aminocaproic acid, indicating that the monoclonal antibody was directed against the hapten-binding site of MOPC 315 IgA. The monoclonal antiidiotypic antibody was of the complement (C)-binding IgG2a subclass and inhibited IgA production and growth of MOPC 315 cells in vitro in the presence of guinea pig C, as assessed by inhibition of formation of plaques and colonies by MOPC 315 cells in agar.
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PMID:A monoclonal antiidiotypic antibody to MOPC 315 IgA inhibits the growth of MOPC 315 myeloma cells in vitro. 745 62

It was found that an antigen-specific IgE response both in vitro and in vivo was strongly suppressed in the presence of IgG1 monoclonal antibody (mAb) against the antigen. Anti-trinitrophenyl (TNP) IgE response was elicited by the co-culture of C3H B-cells and a conalbumin (CA)-specific helper T-cell clone, D10.G4.1, in the presence of 0.1 microgram/ml TNP-CA. Addition of anti-TNP IgG1 monoclonal antibody (mAb) at 1 microgram/ml to the culture resulted in a marked (> 90%) suppression of anti-TNP IgE formation, while anti-TNP IgG1 and IgM responses were affected to a lesser extent (50-60% suppression). Similar observations were made in in vivo experiments. When 100-200 micrograms of anti-TNP IgG1 mAb was injected i.p. into BDF1 mice prior to immunization with TNP-CA, the anti-hapten (TNP) IgE response as well as the IgE response to the carrier (CA) was suppressed by 80-90%, while anti-TNP IgM production was inhibited by less than 50%. Injection of anti-TNP IgM or IgA mAb showed only marginal effects on anti-TNP IgE production. Spleen cells from anti-TNP IgG1 mAb-treated mice cultured in vitro secreted much lower levels of anti-TNP IgE spontaneously than those from untreated mice. In in vitro and in vivo experiments using the F(ab')2 of anti-TNP IgG1 mAb, an IgG1 mAb with an irrelevant specificity and mAb directed to Fc gamma RII, it was shown that the binding of the IgG1 mAb with the antigen and the interaction of its Fc portion with Fc gamma RII are required for the suppressive effects to be exerted.
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PMID:Predominant suppression of anti-TNP IgE response in mice by monoclonal anti-TNP IgG1 antibody: characterization of its mode of action by in vitro and in vivo studies. 784 50